There is a progressive increase in the general background level of mercury in our North American environment. Inorganic mercury in the environment can be converted to organic mercurials in the biological food chain and accumulate in food stuffs, principally as mthylmercury. Methylmercury in humans, unlike inorganic and some other organic mercurials, is widely distributed in body tissues, producing a different pattern of clinical findings than inorganic or elemental mercury. Methylmercury freely passes through the placental barrier. Little is known about the embryopathic effects of chronic mercury intoxication on the primate. The investigation is designed to uncover deleterious effects on the fetus at the level of human "subclinical" exposure. The purpose of this experiment is to determine the threshold level of chronic exposure of pregnant monkeys to methylmercury which produces neurophysiologic deficits in the offspring. Other parameters in the primate such as embryopathic dose range, pathogenesis of the lesions, size of brain and viscera and molecular mechanism of injury. Rodents are used to determine the embryopathic mechanisms. Subsequent completion of the studies in primates will yield information more directly transposable to humans. Findings in the rodents will be tested in congenitally exposed primate infants with respect to physical growth and development as well as the ontogeny of neurobehavioral attributes.